Abstract 011: Regression of Left Ventricle Hypertrophy and Improvement of Ventricular Dysfunction After Renal Revascularization is Dependent of Blood Pressure Response and Etiology of Renal Artery Stenosis

Background: Renovascular hypertension promotes humoral and hemodynamic overload on the cardiovascular system and it is unknown the clinical impact of the correction of renal artery stenosis (RAS) on the structure and function of the heart.We aimed to evaluate the effect of RAS correction on blood pressure (BP) and left ventricle (LV) morphology, function and mass index (LVMI). Methods: Ninety-eight hypertensive patients with significant RAS (> 70%) undergoing percutaneous intervention (26%) or surgical treatment (74%) with a minimum follow-up of 12 months entered the study. We analyzed echocardiographic measurements , including LVMI and ejection fraction (EF) before and after correction of RAS. The BP response after treatment was based on AHA guidelines: cured (BP<140/90 without drugs), improved (BP <140/90 with reduction of number of drugs) and failure. Results: The mean age was 46 ±17 years and 60% were female. The etiology of RAS was atherosclerosis (59%), arteritis (21%) and dysplasia (20%). Before treatment, echocardiography showed LVMI=162 ± 60 g/m2, 73.5% had LV hypertrophy (LVMI > 125 g/m2) and 13 patients had systolic dysfunction (EF<50%). In a mean follow-up of 51 ± 40 months, 62% were considered cured or improved (Benefit group) and 38% as Failure. In the Benefit group, mean LVMI in the follow-up was lower than in Failure group (129 ±44 vs 169 ±42 g/m2, p<.05). The reduction of LVMI was significantly greater in Benefit than in Failure group (23 ±5 vs. 9±9 g/m2, p<.03). The systolic function normalized in 10 from 13 patients with previous dysfunction. The mean LVMI reduction was higher in patients with arteritis than in those with atherosclerosis or dysplasia. Conclusion: Successful renal revascularization promotes significant reduction of LV hypertrophy and normalize previously impaired systolic dysfunction in patients with RAS. The regression of ventricle mass is dependent of BP response after treatment and is more impressive in patients with arteritis.